2001 Fiscal Year Final Research Report Summary
Basic Research for AIDS control A01 ; Host factors necessary for HIV-1 replication
| Project/Area Number |
10180101
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research on Priority Areas (A)
|
| Allocation Type | Single-year Grants |
|---|
| Review Section |
Biological Sciences
|
|---|
| Research Institution | TOHOKU UNIVERSITY (2000-2001)
The University of Tokyo (1998-1999) |
|---|
Principal Investigator |
KOYANAGI Yoshio Tohoku University, Graduate School of Medicine, Professor, 医学系研究科, 教授 (80215417)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
MASUDA Takao Tokyo Medical and Dental University, Medical Research Division, Associate Professor, 医歯学総合研究科, 助教授 (80219336)
OKAMOTO Takashi Nagoya City University, Faculty of Medicine, Professor, 医学部, 教授 (40146600)
SHIODA Tatsuo Osaka University, Research Institute for Microbial Diseases, Professor, 微生物病研究所, 教授 (00187329)
SHIDA Hisatoshi Hokkaido University, Institute for Genetic Medicine, Professor, 遺伝子病制御研究所, 教授 (00144395)
|
|---|
| Project Period (FY) |
1998 – 2001
|
| Keywords | HIV-1 / AIDS / CD4(+) T cell / NF-kappaB / Chemokine receptor / Retrovirus / Integration / Nuclear export |
|---|
| Research Abstract |
Koyanagi reported that TRAIL but not FasL was involved in the apoptotic death of CD4(+) T cells in infected individuals using SCID-PBL mouse system. Furthermore, they showed that TRAIL was also involved in the neuronal cell death in a murine model of HIV central nervous system infection. Shioda identified a deletion mutation in the CCR5 gene specifically seen in Asian population and showed that this mutation affected the surface trafficking of CCR5, resulting in the low sensitivity to HIV-1 infection in the affected individuals. Okamoto identified the host factors essential for viral transcription. One was AES/TLE, as a co-repressor of NF-kappaB p65. Another was FUS/TLS, as a co-activator of NF-kappaB. Masuda found a novel nuclear import signal located in HIV-1 integrase. Shida reported that CRAM1 is necessary for the oligomerization of Rev protein and that human CRAM1 also functioned even in murine cells.
|
